Viral-mediated Overexpression of Neuroligin2 in the Adult Hippocampus Leads to Enhanced Synaptic Inhibition

In this thesis, I explore the effect of using a viral vector AAV to overexpress the inhibitory synaptic protein neuroligin2 (NLGN2) in the hippocampi of adult mice. I hypothesize that NLGN2 is necessary and sufficient to drive the formation of GABAergic synapses in the mammalian adult hippocampus. The goal of my experiments was to use western blot analysis to determine whether AAV-mediated viral delivery of NLGN2 led to concomitant increases in the expression of other proteins localized to the GABAergic synapse. I measured the change in total protein concentration of important inhibitory pre and post-synaptic marker proteins and found that AAV significantly increases expression of NLGN2 in the hippocampus. Moreover, this change in NLGN2 expression is coupled with comparable increases in other inhibitory synaptic proteins. VGAT, an important pre-synaptic inhibitory protein was significantly increased, and gephyrin, an important post-synaptic inhibitory protein was also increased.